We have recently shown that the adult visual cortex retains homeostatic plasticity by showing that short-term monocular deprivation shifts ocular dominance in favor of the deprived eye (Lunghi et al, 2011). Emerging research indicates a strong link between energy metabolism and brain function. For example, obesity is associated with cognitive impairment, neurodegeneration, neuroinflammation, impaired memory and learning and reduced hippocampal plasticity (Guillemot-Legris & Muccioli, 2017). Here we asked whether the impact of obesity affects plasticity in the visual cortex. We measured visual plasticity in healthy adult volunteers, normal-weight or obese (N=51, age: 19-55 years; BMI: 19-54.5), testing binocular rivalry between orthogonal gratings (size: 2°, contrast: 50%, SF: 2cpd) before and after 2h of monocular deprivation. In normal-weight subjects (N=20, BMI=21.17±0.5 kg/m2), the plasticity index (ocular dominance shift after monocular deprivation) is equal to 0.12±0.01. However, we found that it declines sharply for BMI>40 (thethreshold for the diagnosis of class III obesity), where ocular dominance did not change after short-term monocular deprivation (t(16)=0.93, p=0.37) despite normal glucose metabolism and regulation. In addition, across subjects, BMI and the psychophysical plasticity index are strongly negatively correlated (rho=-0.55, p< 0.001). In a subset of these severely obese patients (n=11, BMI=45.7±1.6 kg/m2) that underwent bariatric surgery (gastric bypass), we tested visual plasticity at different times for up to six months following surgery. We found that the effect of monocular deprivation on binocular rivalry steadily increased after surgery (F(3,30)=5.37, p=0.004), indicating that visual plasticity was restored. Six months after surgery, when subjects lost on average 25% of their initial weight (BMI=34.3±1.6 kg/m2), we found a 10-fold increase of the plasticity index, from 0.01±0.03 to 0.1±0.03 (t(10)=3.3, p=0.008), which approached normal values. These results demonstrate a strong influence of energy metabolism on early sensory plasticity and function, though mechanisms accounting for such association remain to be identified.